Therapeutic Intervention against Mitochondria Mediated Inflammation and Its Related Chronic Disorders

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 March 2024 | Viewed by 1535

Special Issue Editors

Department of Pharmaceutical Sciences, School of Pharmacy, University of Maryland Eastern Shore, Princess Anne, MD, USA
Interests: mitochondria; inflammation; chronic disease; cancer metastasis; neurodegenerative disease; apoptosis; ion channel modulation
Special Issues, Collections and Topics in MDPI journals
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia
Interests: cancer metastasis; oxidative stress; inflammation; antioxidants
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia
Interests: cardiovascular diseases (ischemic heart diseases); ischemia reperfusion (IR) injury; inflammatory response; mechanisms of cardiotoxicity induced by different anti-cancer drugs

Special Issue Information

Dear Colleagues,

Mitochondria have recently developed as a key organelle and regulate cellular functions including cell proliferation or differentiation, cell death, metabolism, and cellular signaling, considered for inflammation-mediated diseases. Mitochondrial-evolved ROS has been implicated as a mediator for redox signaling, thereby causing stimulation of inflammatory proteins followed by mitochondrial deterioration and oxidative stress. Due to this kind of oxidative damage, chronic inflammation is believed to provoke several chronic diseases, including cancer and neurodegenerative disorders. In recent years, a promising insight into mitochondria-mediated cell death and inflammation has shed light on the molecular signature of the signaling machinery that could mediate different cascades of cell death and multiple kinds of inflammatory responses in chronic disease. Impairment of mitochondria-mediated anti-inflammatory machinery could cause an aggregation of unhealthy cellular components, followed by mitochondria-mediated cell death and its related episodes. To eradicate such cellular issues, and to explore whether novel strategies may be challenging therapeutic interventions, enriched delivery of the drugs and/or molecules to the impaired cells of patients with mitochondria-mediated chronic disorder is warranted. This Special Issue of Biomedicines aims to collect the original research articles and comprehensive reviews considering probable significance or impacts of pharmacotherapeutics on mitochondria-mediated inflammation and its mediated disease resistance in scientific community and healthcare settings.

Dr. Mohammad Waseem
Dr. Nemat Ali
Dr. Abdullah F. AlAsmari
Guest Editors

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Keywords

  • mitochondrial dysfunction
  • inflammatory response
  • chronic disorder
  • cell death
  • novel drugs
  • pharmacological intervention
  • cancer
  • neurodegenerative disorder

Published Papers (1 paper)

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Research

16 pages, 3410 KiB  
Article
Preventive Action of Beta-Carotene against the Indoxyl Sulfate-Induced Renal Dysfunction in Male Adult Zebrafish via Regulations of Mitochondrial Inflammatory and β-Carotene Oxygenase-2 Actions
by Arunachalam Muthuraman, Abu Sadat Md. Sayem, Sakthiganapathi Meenakshisundaram, Nemat Ali, Sheikh F. Ahmad, Abdullah F. AlAsmari, Shamama Nishat, Khian Giap Lim and Yamunna Paramaswaran
Biomedicines 2023, 11(10), 2654; https://doi.org/10.3390/biomedicines11102654 - 27 Sep 2023
Viewed by 984
Abstract
Indoxyl sulfate (IS) is a metabolic byproduct of indole metabolism. IS readily interacts with the mitochondrial redox metabolism, leading to altered renal function. The β-carotene oxygenase-2 (BCO2) enzyme converts carotenoids to intermediate products. However, the role of β-carotene (BC) in IS-induced renal dysfunction [...] Read more.
Indoxyl sulfate (IS) is a metabolic byproduct of indole metabolism. IS readily interacts with the mitochondrial redox metabolism, leading to altered renal function. The β-carotene oxygenase-2 (BCO2) enzyme converts carotenoids to intermediate products. However, the role of β-carotene (BC) in IS-induced renal dysfunction in zebrafish and their modulatory action on BCO2 and mitochondrial inflammations have not been explored yet. Hence, the present study is designed to investigate the role of BC in the attenuation of IS-induced renal dysfunction via regulations of mitochondrial redox balance by BCO2 actions. Renal dysfunction was induced by exposure to IS (10 mg/L/hour/day) for 4 weeks. BC (50 and 100 mg/L/hour/day) and coenzyme Q10 (CoQ10; 20 mg/L/hour/day) were added before IS exposure. BC attenuated the IS-induced increase in blood urea nitrogen (BUN) and creatinine concentrations, adenosine triphosphate (ATP), and complex I activity levels, and the reduction of renal mitochondrial biomarkers, i.e., BCO2, superoxide dismutase-2 (SOD2), glutathione peroxidase-1 (GPX1), reduced and oxidized glutathione (GSH/GSSG) ratio, and carbonylated proteins. Moreover, renal histopathological changes were analyzed by the eosin and hematoxylin staining method. As a result, the administration of BC attenuated the IS-induced renal damage via the regulation of mitochondrial function. Full article
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